Table 4.

Joint association of NSAID use and Ptgs2 rs5275 genotype with invasive ovarian carcinoma risk

NSAID use	No. (%) cases by genotype			No. (%) controls by genotype			OR (95% CI)*			P	P§
	TT	TC	CC	TT	TC	CC	TT	TC	CC
	HAWAII and NECC studies combined (940 cases/1514 controls)
Nonusers	282 (30)	235 (25)	65 (7)	375 (25)	354 (23)	98 (6)	1.00 (reference)	0.86 (0.68-1.08)	0.85 (0.60-1.22)
Aspirin	65(7)	54 (6)	17 (2)	118 (8)	92 (6)	17 (1)	0.72 (0.50-1.02)	0.74 (0.51-1.08)	1.21 (0.60-2.44)
Nonaspirin	64 (7)	67 (7)	9 (1)	157 (10)	103 (7)	32 (2)	0.61 (0.43-0.85)	0.97 (0.68-1.38)	0.43 (0.20-0.93)
Both groups	39 (4)	36 (4)	7 (1)	73 (5)	70 (5)	25 (2)	0.70 (0.45-1.07)	0.68 (0.43-1.07)	0.42 (0.18-1.01)	0.05 †	0.09
Any NSAID	172 (18)	160 (17)	34 (4)	361 (24)	269 (18)	75 (5)	0.67 (0.52-0.86)	0.81 (0.63-1.05)	0.63 (0.40-0.99)	0.04 ‡	0.16
¶Pfor heterogeneity of the effects of genotype and NSAID use by type between studies										0.37
¶Pfor heterogeneity of the effects of genotype and any NSAID use between studies										0.51

^*ORs and 95% CIs adjusted for age, ethnicity, education, family history of breast and/or ovarian cancer, menopausal status, use of contraceptive and menopausal hormones and, in combined analysis, study

^†P global (11 d.f) from the multivariate logistic regression models comparing joint effect of rs5275 genotype and NSAID use by group

^‡P global (5 d.f.) from the multivariate logistic regression models comparing joint effect of rs5275 genotype and any NSAID

^§P for interaction of rs5275 with risk by strata of NSAID use was calculated using Wald test for the genotype-stratum interaction terms

^¶P for heterogeneity of the effects of NSAID use and genotype by study was calculated using Wald test for the genotype-study interaction terms

Note: statistically significant estimates (p<0.05) are presented in bold font